mProX™ Human PDK2 Stable Cell Line

Sheng, Ning. et al. "Scutellarin Rescued Mitochondrial Damage through Ameliorating Mitochondrial Glucose Oxidation via the Pdk-Pdc Axis." Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2023.
In their research, the authors investigated the effects of a small molecule, scutellarin (SG), on mitochondrial bioenergetic deficits and glucose hypometabolism, which are known to promote neurodegeneration. They observed that SG was able to alleviate neuropathological changes in the hippocampal CA1 region of rat models of cerebral hypoperfusion. Furthermore, SG also restored mitochondrial homeostasis by repairing mitochondrial damage and regulating energy metabolism. Their findings suggest that SG could be a potential treatment for neurological diseases by targeting the pyruvate dehydrogenase (PDH) complex and its phosphorylation by pyruvate dehydrogenase kinase (PDK). This was supported by mitochondrial proteomics, energy metabolism monitoring, and isotope tracing analyses. Ultimately, these results highlight the importance of targeting mitochondrial function in the treatment of neurological diseases.
Sheng, Ning. et al. "Scutellarin Rescued Mitochondrial Damage through Ameliorating Mitochondrial Glucose Oxidation via the Pdk-Pdc Axis." Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2023.
Pubmed: 37750289   DOI: 10.1002/advs.202303584

Guo, Yongjian. et al. "Inhibition of mitochondrial fusion via SIRT1/PDK2/PARL axis breaks mitochondrial metabolic plasticity and sensitizes cancer cells to glucose restriction therapy." Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2023.
The study focuses on the role of mitochondrial dynamics in cancer development and the potential for targeting this process in cancer therapy. The researchers identified a compound called oroxylin A (OA) that inhibits both glucose metabolism and mitochondrial fusion in hepatocellular carcinoma cells. They found that cancer cells with healthy mitochondria and high spare respiratory capacity (SRC) were more resistant to glucose restriction therapy due to their ability to adapt and fuse mitochondria. However, inhibiting mitochondrial fusion increased their susceptibility to glucose restriction treatment. These findings suggest that combining a GLUT1 inhibitor with a mitochondrial fusion inhibitor could be a promising approach for cancer therapy. This study highlights the importance of considering both mitochondrial dynamics and metabolic regulation as potential vulnerabilities in cancer treatment.
Guo, Yongjian. et al. "Inhibition of mitochondrial fusion via SIRT1/PDK2/PARL axis breaks mitochondrial metabolic plasticity and sensitizes cancer cells to glucose restriction therapy." Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2023.
Pubmed: 37633053   DOI: 10.1016/j.biopha.2023.115342